Session 10 - Drugs Rate and Rhythm Flashcards Preview

Semester 5 - Farmocology > Session 10 - Drugs Rate and Rhythm > Flashcards

Flashcards in Session 10 - Drugs Rate and Rhythm Deck (62)
1

What is the cardiac resting membrane potential?

-90mV

2

What sets the resting membrane potential for cardiac cells?

The relative permeability of the cardiac myocyte to K+

3

What is the equilibrium potential of K+?

-80mV

4

Outline a contraction of a ventricular myocyte?

o In diastole, the resting membrane potential of cardiac cells is close to the equilibrium potential of K+ (4).
o Initial depolarisation due to spread of electrical activity from pacemaker cells. Once threshold has been reached, fast voltage gated sodium channels are opened, causing depolarisation towards Na+’s equilibrium potential (0).
o Following the rapid depolarisation, a brief repolarisation caused by the outward flow of K+ returns the membrane potential to ~0. (1)
o Na+ channels deactivate, but the depolarisation causes the opening of voltage gated Ca2+ channels, which take longer to activate, keeping the membrane depolarised (2).
o Influx of Ca2+ causes the release of further Ca2+ from cellular stores, causing contraction (See M&R Session 5).
o After ~250ms, Ca2+ channels close.
o Efflux of K+ returns membrane potential to resting (3).

5

Give the classification of anti-arythmic drugs

Class 1 - Na+ blockes
Class 2 - B blocekrs
Class 3 - K+ channel blockers
Class 4 - Ca2+ channel blockers

6

Give three types of Na+ channel blockers

1a) Quinidine
1b) Lidocaine
1c) Felcainide

7

Give a type of beta blocker

Atenolol
Bisoprolol
Metoprolol

8

Give a widely used K+ channel blocker

Amiodarone

9

Give a Ca2+ channel blocker

Verapamil

10

What are the effects of Flecainide and Lidocaine?

Decrease conduction velocity
Increase depolarisation threshold
Decrease automacity

11

What is the route of administration of flecainide?

Oral and intravenous

12

What are the indications for flecinaide?

Supraventricular tachyarrythmias (atrial arrhythmia)

13

Give two contraindications for Flecainide?

Heart failure, History of MI

14

What is the mechanism of action for Flecainide?

Blocks fast, inward Na+ ion channel (Phase 0)

15

Give three adverse reactions of flecainide

 Dizziness, visual disturbances, arrhythmias

16

What are the drug-drug interactions for Flecainide?

 Metabolised by CYP2D6 and eliminated renally. Inducers/inhibitors

17

How is lidocaine adminstered?

Intravenously

18

What are the indications for lidocaine?

Ventricular arrhythmias following MIO

19

What are the contraindications for Lidocaine (2)

AV block
Heart failure

20

Give three adverse drug reactions for lidocaine

Hypotension, bradycardia
Nystagmus
Seizures

21

What do beta blockers act on?

B1 receptors in the heart

22

What is the action of B blockers

Block sympathetic action
Decrease slop of pacemaker potential in SAN
Decrease chronotrophy
Inhibits adenyl cyclase, decrease inotrophy

23

What do B blockers do to ventricular action potential?

Shifts it to the right

24

What are the indications for B blockers? (4)

 Angina
 Post myocardial infarction
 Hypertension
 Arrhythmias

25

What are the two main contraindications for beta blockers?

Asthma
General decreased heart function

26

What is the mechanism of action for beta blockers?

 Antagonise β-adrenoreceptors. β1-receptors are found in the heart, when they are activated they cause increased Chronotropy and Inotropy.
 Inhibits renin release

27

Give some adverse drug reactions for beta blockers

 Bronchospasm, fatigue and insomnia, dizziness, cold extremities, hypotension, bradycardia and decreased glucose tolerance in diabetic patients – Don’t feel adrenaline from hypoglycaemia due to B blockers, dangerous

28

Give two drug-drug interactions of Beta blockers

 Prevents Salbutamol working (β2-adrenoagonist)
 Verapamil – Both have –‘ve inotropic action

29

What do K+ channel blockers do?

Prolong the absolute refractory period by increase AP duration
Also suppress re-entry circuits by closing excitable gap

30

Why are they not generally used?

Torsades de pointes

31

Give an example of a potassium channel blocker

Amiodarone

32

What is the route of administration of potassium channel blockers?

Oral or intravenous

33

What are the indications for potassium channel blockers

Ventricular and supraventricular arrythmia

34

What are some drug-drug interactions of amiodarone?

Inhibits CYP3A4, CYP2C9 and P-glycoprotein
 Dose reductions of Warfarin, Digoxin, Flecainide needed

35

What do Ca2+ blockers do?

Increased refractory period
Decreased Chronotrophy and Inotropy

36

Give two examples of Calcium channel blockers

Verapamil
Diltiazem

37

Give a route of admin for calcium

Oral

38

Give three indications for Ca2+ blockers

Supraventriuclar arrhythmias
Prophylaxis and treatment of angina nad hypertension

39

Give three contraindications for Calcium channel blockers

Heart failure
Bradycardia
AV node block

40

Give four adverse reactions to calcium channel blockers?

Hypotension
Bradycardia
Heart failure
Heart block

41

What is used to treat torsades de pointes?

Digoxin
Adenosine

42

What does adenosine do?

Blocks AV node

43

What are the two main effects of adenosine?

Decrease automacity
Increased AVN refractory period

44

What are two main indications for digoxin?

Supraventricular arrhythmias, Heart Failure

45

Give two contraindications for digoxin

Heart block
Hypokalaemia

46

Outline the mech of action of digoxin

o Inhibits Na/K-ATPase
o Direct Cardiac Effects
  Inotrope – Used in heart failure, no mortality benefit
o CNS Effects
  Sympathetic outflow
  Parasympathetic outflow
 Sensitises baroreceptor reflex
o Combined Effects
  Automaticity of SAN and AVN
  AVN refractory period
  Conduction velocity of AVN

47

What are three adverse drug reactions to digoxin?

o Narrow therapeutic index
o Toxicity enhanced with hypokalaemia
o Cardiac toxicity – bradycardia, AVN block, atrial tachycardia

48

Give some drugs which increase digoxin levels

Popafenone, Quinidine, Amiodarone, Verapamil, Spironolactone, Cylosporine

49

Give some drugs which decrease digoxin levels

Erythromycin, Tetracycline (gut bacteria metabolise digoxin)

50

Why do you split loading dose of digoxin in two?

To minimise toxicity risk

51

How much of digoxin is protein bound

20-30%

52

What is digoxin clearance proportional to?

GFR

53

Give three examples of ACE inhibitors

 Ramipril
 Lisinopril
 Captopril

54

Give three indications for ACE inhibitors

 Hypertension
 Heart failure
 Renal dysfunction

55

Give three contraindications for ACE inhibitors

Pregnancy
Renovascular
Aortic stenosis

56

Outline mech of action of ACE inhibitors

 ACE inhibitors cause inhibition of Angiotensin Converting Enzyme, consequently reducing Angiotensin II and Aldosterone levels. This causes vasodilation and consequent reduction in peripheral resistance and reduced sodium retention.
 Reduce breakdown of the vasodilator Bradykinin

57

Give five adverse reactions of ACE inhibitors

 Characteristic dry cough
 Angio-oedema (rare, but more common in black population)
 Renal Failure
 Hyperkalaemia
 Hypotension, dizziness and headache, diarrhoea and muscle cramps

58

Give two angiotensin blockers

Losartan
Valsartan

59

What is an indication for angiotensin blocker?

Hypertension

60

Give four contraindications

 Pregnancy, breastfeeding
 Caution in renal artery stenosis and aortic stenosis

61

What is the mech of action of angiotensin blocker?

 Bind to and antagonise the receptor for Angiotensin II – Angiotensin 1 Receptor (AT1 R).
 Inhibits vasoconstriction and aldosterone stimulation by angiotensin II.

62

Give two adverse drug reactions to angiotensin receptor blockers

 Renal failure
 Hyperkalaemia